Implantable neurostimulation systems have proven therapeutic in a wide variety of diseases and disorders. Pacemakers and Implantable Cardiac Defibrillators (ICDs) have proven highly effective in the treatment of a number of cardiac conditions (e.g., arrhythmias). Spinal Cord Stimulation (SCS) systems have long been accepted as a therapeutic modality for the treatment of chronic pain syndromes, and the application of tissue stimulation has begun to expand to additional applications such as angina pectoralis and incontinence. Deep Brain Stimulation (DBS) has also been applied therapeutically for well over a decade for the treatment of refractory chronic pain syndromes, and DBS has also recently been applied in additional areas such as movement disorders and epilepsy. Further, Functional Electrical Stimulation (FES) systems such as the Freehand system by NeuroControl (Cleveland, Ohio) have been applied to restore some functionality to paralyzed extremities in spinal cord injury patients. Furthermore, in recent investigations Peripheral Nerve Stimulation (PNS) systems have demonstrated efficacy in the treatment of chronic pain syndromes and incontinence, and a number of additional applications are currently under investigation. Specifically, Occipital Nerve Stimulation (ONS), in which leads are implanted in the tissue over the occipital nerves, has shown promise as a treatment for various headaches, including migraine headaches, cluster headaches, and cervicogenic headaches.
Each of these implantable neurostimulation systems typically includes an electrode lead, having one or more electrodes, implanted at the desired stimulation site and an implantable pulse generator (IPG) implanted remotely from the stimulation site, but coupled either directly to the electrode lead or indirectly to the electrode lead via a lead extension. Thus, electrical pulses can be delivered from the IPG to the electrode lead to stimulate the tissue and provide the desired efficacious therapy to the patient.
Significantly, precise positioning of the leads proximal to the targets of stimulation is critical to the success of the therapy. If the leads shift position, the stimulation target tissue may no longer be appropriately stimulated. For example, when electrical stimulation devices, such as occipital nerve stimulators, are implanted in a patient, the leads and the IPG are anchored to the tissue. However, during postural changes and patient movement, the leads (and/or other system components) may shift. Notably, in lead shifting, as opposed to lead migration, the leads return to their previous position after the patient returns to a neutral/resting position.
During lead shifting, the patient feels a change in stimulation sensations and possibly no stimulation at all. Changes in stimulation sensation may be drastic, causing jolting or a piercing sensation. When lead shifting eliminates paresthesia, i.e. the tingling sensation that replaces pain during successful treatment, the patient may revert back to their pain state, or, in the case of ONS, generate a migraine headache.
Changes in stimulation may be explained by the lead moving back and forth over the targeted nerve, while removal of stimulation therapy may be explained by the lead shifting off of the nerve. The entire lead may not shift off of the nerve. Instead, one stimulating electrode may shift off of the nerve or shift too far away from the nerve for effective stimulation. For instance, when an ONS patient's head is rotated, implanted stimulating electrodes may no longer be properly positioned over the targeted occipital nerves.
Changes in stimulation with posture change can also be caused by changes in the thickness of the tissue between the lead and the targeted nerve. The thickness of this intervening tissue may decrease when postural changes, such as neck movements, stretch the tissue or increase when postural changes bunch up the tissue. This change in thickness of the intervening tissue, in turn, moves the lead closer to or farther from the targeted nerve, resulting in changes in stimulation.
Lead shifting can be overcome by reprogramming the tissue stimulation system based on the new position of the leads to restore therapy. However, determining the presence and degree of lead shifting based paresthesia is imprecise. Also, attempting to reprogram the leads based on paresthesia locations is challenging.
Alternatively, a determination of the position of implanted leads can be made using X-ray or fluoroscopy. Disadvantageously, X-ray and fluoroscopy require expensive equipment, significant time, and appropriate medical facilities, most of which are not readily available. Moreover, if the leads shift after a fluoroscopic image is taken, this image may no longer be valid, thereby resulting in poor patient outcomes due to inappropriate or unexpected stimulation effects.
There, thus, remains a need for an improved method and system for compensating for lead shifting during patient movement.